A recent study in Cell reported on experiments regarding mitochondrial function and amyloid protein accumulation in the muscles.[ref]
The researchers used animal models and human muscle tissue to determine that amyloid-like protein deposits occur in muscle during aging. Amyloid proteins are aggregates of proteins that fold into long fibers. Perhaps the most well-known is amyloid-beta, which is the amyloid version of the APP protein and commonly found in Alzheimer’s brains.
Additionally, the researchers confirmed previous research showing a decline in mitochondrial function. Together, the amyloid proteins and reduced mitochondrial function “may represent a major common hallmark of muscle aging and disease.”
NAD+ also declines in muscle tissue in aging. The researchers showed that blocking the NAD+ salvage pathway, which reduced NAD+ in the cells, robustly induced the muscle cells to produce amyloid protein aggregations.
The opposite also seems to be true – boosting NAD+ attenuated the formation of amyloid protein aggregates in aging cells.
In an animal model, boosting NAD+ in older cells may reduce the amyloid deposits. The researchers tested nicotinamide riboside (NR) and olaparib (AZD). Nicotinamide riboside is commonly available as a supplement, and olaparib is a PARP inhibitor used for cancer treatment. Both were successful at ameliorating amyloid deposits in the muscle cells.
Why is this a big deal?
Loss of muscle mass in aging can lead to devastating health effects such as falling and breaking a hip. Oddly enough, researchers don’t really know what all goes into the loss of muscle in aging. This research is important both in pointing out mechanisms as well as a possible solution.
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